By Roberta Attanasio
Redness, heat, swelling, pain – these are the four well known signs of the inflammatory response. Although a bit uncomfortable, these signs let us know that our immune system is working hard to get rid of microorganisms or other harmful agents while repairing tissue damage. Once the job is done, the immune system goes back to its steady-state, ready to fight again whenever the need arises.
However, the inflammatory response itself can sometimes be damaging. One type of damaging response leads to the development of degenerative diseases, as for example diabetes, cardiovascular disease and cancer. This type of response – chronic inflammation – may be triggered by a variety of factors. and childhood poverty is one of them. Indeed, results from several studies carried out in the past few years indicate that low childhood socioeconomic status is linked to a variety of health problems in adult age.
Gregory Miller and Edith Chen, both at The Center on Social Disparities and Health, Institute for Policy Research, Northwestern University, propose a novel, provocative model to explain the link between childhood poverty and health problems in adult age. The model includes social and physical pollutants that, together, enable childhood disadvantage to become embedded in the function of monocytes and macrophages, which represent two different maturation stages of the same cell type and play a major role in orchestrating the immune response.
Known examples of social and physical pollutants, also called “anthropogens“, are unstable family structures, unresponsive caregivers and neighborhood violence. In addition, low socioeconomic status children are likely to experience household crowding, inadequate nutrition, and more exposure to second-hand smoke, infectious microorganisms, and industrial pollutants.
According to the model, clearly articulated in a recent article entitled “The biological residue of childhood poverty” and published in the journal Child Development Perspectives, these pollutants enable disadvantage to become embedded in the function of monocytes and macrophages – in other words, because exposure to pollutants occurs during a sensitive period of immunological development, these cells acquire a pro-inflammatory phenotype, and this phenotype persists across the lifespan.
Thus, childhood poverty induces persistent inflammation, which is known to foster pathogenic changes that lead to degenerative diseases. According to the model, such process is reinforced by the acquired resistance of monocytes and macrophages to anti-inflammatory signals. Furthermore, early childhood disadvantage not only promotes a pro-inflammatory phenotype, it also gives rise to a behavioral predisposition that continuously accentuate this tendency.
In conclusion, Miller and Chen propose that childhood disadvantage leaves an “immunologic residue“. This immunologic residue manifests in pro-inflammatory responses and resistance to anti-inflammatory signals. It should be noted, however, that the research at the basis of this model is based on children that live in high income Western countries. In developing countries, where poverty is more common and extreme, the pathways of vulnerability may be different.